ライフサイエンスコーパス: eGFR

1 eGFR < 30 ml/min/1.73 m(2) [OR 3.641, 95% CI 1.572-8.433

2 eGFR and albuminuria contributed multiplicatively (eg, a

3 eGFR did not change in either group.

4 eGFR was assessed by using the Chronic Kidney Disease Ep

5 eGFR was modeled in a time-varying linear mixed-effects

6 n categories of coffee and tea intake and 1) eGFR and 2) subsequent annual changes in eGFR by using g

7 A >/=20% eGFR decline associated with higher risk of ESRD in both

8 FR decline in the usual BP arm, a 5% to <20% eGFR decline during intensive BP lowering did not associ

9 However, a 5% to <20% eGFR decline in the usual BP arm associated with higher

10 The regions containing the 243 eGFR-associated (P < 1e-05) CpGs are significantly enric

11 D as eGFR<60 ml/min per 1.73 m(2) and >/=30% eGFR decline at the third visit (2009-2013) relative to

12 1.29), CKD (HR, 1.27; 95% CI, 1.17 to 1.38), eGFR decline >/=30% (HR, 1.28; 95% CI, 1.18 to 1.39), an

13 Compared with a <5% eGFR decline in the usual BP arm, a 5% to <20% eGFR decl

14 nt of CKD progression was a composite of 50% eGFR loss, eGFR less than 10 mL/min/1.73 m2, or initiati

15 between race/ethnicity, CKD progression (50% eGFR loss or incident ESRD), incident ESRD, and all-caus

16 After age 70, eGFR declined.

17 Thus, acute eGFR declines >/=20% during intensive BP lowering identi

18 Patients with ADPKD, eGFR>/=60 ml/min per 1.73 m(2), and total kidney volume

19 an association between CFHR3,1Delta and age, eGFR, urinary protein excretion rate, or the presence of

20 1 nondiabetic participants with ADPKD and an eGFR>60 ml/min per 1.73 m(2) who participated in the Hal

21 min per 1.73 m(2) and 2.06 (1.70-2.48) at an eGFR of 15 mL/min per 1.73 m(2).

22 ry disease was 1.22 (95% CI 1.14-1.30) at an eGFR of 45 mL/min per 1.73 m(2) and 2.06 (1.70-2.48) at

23 corresponding increase in CKD (defined by an eGFR<60 ml/min per 1.73 m(2)) has been shown to associat

24 lant >/=6 months before the study and had an eGFR>30 ml/min per 1.73 m(2) The primary end point was t

25 who received young DBD or DCD kidneys had an eGFR<30 ml/min per 1.73 m(2) (including primary nonfunct

26 follow-up, 68% of PEPT2*1*1 carriers had an eGFR<60 ml/min per 1.73 m(2), compared with 37% of PEPT2

27 An increased risk of an eGFR decline of 30% or more was associated with an IQR i

28 he start of renal replacement therapy, or an eGFR less than 10 mL/min/1.73 m2.

29 on (59.0%, 385 of 653) were classified to an eGFR category indicating more severe CKD.

30 Compared with an eGFR of 95 mL/min per 1.73 m(2), adjusted hazard ratios

31 *1 genotype independently associated with an eGFR<60 ml/min per 1.73 m(2) (odds ratio, 6.85; 95% conf

32 e mean+/-standard deviation baseline age and eGFR of HF patients were 68+/-11 years and 78+/-14 mL mi

33 eceptor blockers with well controlled BP and eGFR<90 ml/min per 1.73 m(2), to receive standard therap

34 mellitus, prior cardiovascular disease, and eGFR.

35 suPAR level was measured at enrollment, and eGFR was measured every 2 months in the ESCAPE Trial and

36 adjustment for urinary albumin excretion and eGFR [HR:1.15 (95% CI, 0.81-1.64),Ptrend = 0.22].

37 Menopause and eGFR were significantly associated with measured (trend

38 associations between single metabolites and eGFR.

39 In addition to age, sex, and eGFR, T50 improved prognostication for all-cause mortali

40 placebo or bosutinib had similar annualized eGFR decline.

41 n/1.73 m2, and a confirmed (>3 months apart) eGFR < 60 ml/min/1.73 m2 thereafter to calculate CVD and

42 e was defined as confirmed (>3 months apart) eGFR lower than 60 mL/min per 1.73 m(2).

43 We defined incident CKD as eGFR<60 ml/min per 1.73 m(2) and >/=30% eGFR decline at

44 ts with prevalent kidney disease (defined as eGFR <60 mL.min(-1).1.73 m(-2) and/or urine albumin-crea

45 >30 mg/g, and CKD stages 3-5 was defined as eGFR<60 ml/min per 1.73 m(2) CKD prevalence was age- and

46 CKD stages 1-5 was defined as eGFR<60 ml/min per 1.73 m(2), as calculated by the CKD-E

47 in individuals with CKD seems to diminish as eGFR declines.

48 fference in treatment effect was observed at eGFR</=75 ml/min per 1.73 m(2) and most apparent at leve

49 ecade correlated with time trends in average eGFR at 1 year after kidney transplant in the United Sta

50 We calculated the average eGFR at 1 year after transplant for the recipient cohort

51 ssessed the impact of using cystatin-C-based eGFR in risk prediction equations for CKD progression an

52 to quantify associations of creatinine-based eGFR, urine albumin-to-creatinine ratio (ACR), and dipst

53 Baseline eGFR did not differ significantly by mtDNA copy number.

54 5% CI], 0.82 to 0.95); those with a baseline eGFR of 45 ml/min per 1.73 m(2) had a 13% risk reduction

55 eceiving combination therapy with a baseline eGFR of 60 ml/min per 1.73 m(2) experienced a 12% risk r

56 yses were performed in subgroups by baseline eGFR (<45, 45-<60, 60-<90, >/=90 mL.min(-1).1.73 m(-2))

57 r sociodemographic characteristics, baseline eGFR, comorbidities, body mass index, SBP, diastolic BP,

58 plete risk factor (covariate) data, baseline eGFR > 60 ml/min/1.73 m2, and a confirmed (>3 months apa

59 e adjusted models for demographics, baseline eGFR, urine albumin-to-creatinine ratio, comorbidity, an

60 Participants had a median baseline eGFR of 110 mL/min per 1.73 m(2) (IQR 100-125), a median

61 dels included age, sex, black race, baseline eGFR, and baseline proteinuria.

62 eline among those participants with baseline eGFR >/=60 ml/min per 1.73 m(2) At baseline, mean age wa

63 In patients with baseline eGFR greater than 40 mL/min/1.73 m2, higher log-transfor

64 Both eGFR and ACR significantly improved peripheral artery di

65 participants with or without CKD (defined by eGFR), FGF23 concentration associated with first infecti

66 was performed on kidney function (defined by eGFR), HDL-cholesterol and triglycerides.

67 herapy compared with monotherapy differed by eGFR (P=0.04).

68 ation of TMAO with mortality was modified by eGFR in crude and age- and sex-adjusted analyses (intera

69 0 mL/min/1.73 m(2)), those with stage 3 CKD (eGFR, 30-59 mL/min/1.73 m(2)), and those with stage 4-5

70 in/1.73 m(2)), and those with stage 4-5 CKD (eGFR < 30 mL/min/1.73 m(2)) and separately underwent pro

71 in women with r-AKI without history of CKD (eGFR>90 ml/min per 1.73 m(2) before conception; n=105) w

72 ssociations differed by the presence of CKD (eGFR<60 ml/min per 1.73 m(2) [n=832] or urine albumin-to

73 ive cohort of 2568 participants without CKD (eGFR>60 ml/min per 1.73 m(2)) at baseline.

74 d risk of eGFR<60 ml/min per 1.73 m(2), CKD, eGFR decline >/=30%, and ESRD.

75 eGFR <60 ml/min per 1.73 m(2), incident CKD, eGFR decline >/=30%, and ESRD over a median follow-up of

76 exposure to PM2.5 and risk of incident CKD, eGFR decline, and ESRD.

77 Among participants with CKD, eGFR did not significantly correlate with insulin sensit

78 Multivariable analyses confirmed eGFR and albuminuria as key risk factors for predicting

79 ade 1: n = 3, grade 3: n = 1) but creatinine/eGFR returned to baseline values in all patients.

80 line: eGFR decline >/=30%; absolute decline: eGFR decline >3 ml/min per year) and incident CKD (incid

81 ecline in kidney function (relative decline: eGFR decline >/=30%; absolute decline: eGFR decline >3 m

82 In individuals with a mildly decreased eGFR, higher consumption of milk, milk products, and low

83 pro-ENK) have been associated with decreased eGFR in an acute setting.

84 1.73 m(2), incident chronic kidney disease, eGFR decline of 30% or more, and end-stage renal disease

85 sed risk of incident chronic kidney disease, eGFR decline, and end-stage renal disease.

86 ata suggests that postdonation, kidney donor eGFR increases each year for a number of years and that

87 Primary outcomes were incident ESRD, eGFR slope, log-transformed UPCR slope, and all-cause de

88 umarate) were also more likely to experience eGFR decline and worsening albuminuria compared with HIV

89 r demographics, cardiovascular risk factors, eGFR, and urine albumin-to-creatinine ratio.

90 idence interval [CI], -0.79 to -0.21) faster eGFR decline.

91 sis, the only independent predictor of final eGFR was initial eGFR, highlighting the importance of ea

92 oss-sectional associations were assessed for eGFR and menopause (yes/no).

93 e in the instrumental variable estimator for eGFR (P<0.01) in a Mendelian randomization analysis.

94 r (ETV) and to assess predictive factors for eGFR improvement.

95 I) was the most accurate published model for eGFR (RMSE, 16.30 mL/min; 95% CI, 15.34 to 17.38 mL/min)

96 or near-normal preoperative kidney function (eGFR>/=60 ml/min per 1.73 m(2)), partial nephrectomy was

97 function from 93%-95% with normal function (eGFR>/=90 ml/min per 1.73 m(2); n=722) to 57%-61% with s

98 ticipants were stratified by renal function (eGFR < vs. >/=90 mL/min/1.73 m(2)), TMAO was associated

99 %-61% with severely impaired renal function (eGFR<30 ml/min per 1.73 m(2); n=81) and 40%-41% on dialy

100 0.01) along with better transplant function (eGFR 65+/-19 versus 50+/-24 ml/min per 1.73 m(2), P<0.00

101 DTA GFR was compared with the estimated GFR (eGFR) from seven published models and our new model, usi

102 oint was percentage change in estimated GFR (eGFR) trajectory over the treatment period.

103 h CKD G3a or G3b defined by 2 estimated GFR (eGFR) values more than 90 days apart were recruited to t

104 RT was independently associated with greater eGFR decline (-0.56; 95% CI = -0.87 to -0.24 mL/min/1.73

105 n (per 1% more) each associated with greater eGFR decline (-1.12 and -0.18 ml/min per 1.73 m(2) per y

106 y also independently associated with greater eGFR decline (slope) versus normal weight (fully adjuste

107 en was modified, was associated with greater eGFR decline or worsening albuminuria (increase >/=10%/y

108 100 mg, and canagliflozin 300 mg groups had eGFR declines of 3.3 ml/min per 1.73 m(2) per year (95%

109 ients with not only lower but also very high eGFR.

110 es with lower renal PTPN6 expression, higher eGFR, and less renal fibrosis.

111 n with eGFR changes suggests that the higher eGFR among coffee consumers is unlikely to be a result o

112 eit significant association with the highest eGFR category emerged.

113 In adjusted models using the highest eGFR/lowest ACR grouping as the referent, patients with

114 However, eGFR was not associated with cortical thickness.

115 r 4, 48.8 and 21.3% patients had an improved eGFR from baseline in LdT and ETV patients, respectively

116 The treatment group had an improved eGFR trajectory versus control, based on our predetermin

117 While improved eGFR did not improve 1-year outcomes, worsening eGFR was

118 Patients were categorized with improved eGFR (30-day follow-up eGFR>/=10% higher than baseline p

119 The group with improved eGFR had more women, nonsmokers, and a lower cardiac ind

120 From 30 days to 1 year, those with improved eGFR had no difference in mortality or repeat hospitaliz

121 An increase of more than 10% in eGFR from the baseline was identified as an improvement.

122 ase and 10.61 [5.70-19.77] for amputation in eGFR <30 mL/min per 1.73 m(2) plus ACR >/=300 mg/g or di

123 roup had a slightly higher rate of change in eGFR (-0.47 versus -0.32 ml/min per 1.73 m(2) per year;

124 End points were annual change in eGFR and albuminuria over 2 years of follow-up.

125 st was CKD progression measured as change in eGFR over time among 1331 blacks and 1476 whites with CK

126 included change in proteinuria and change in eGFR.

127 1) eGFR and 2) subsequent annual changes in eGFR by using generalized estimating equation analyses.

128 a consumption was associated with changes in eGFR.

129 The predictor was the percentage decline in eGFR (<5%, 5% to <20%, or >/=20%) between randomization

130 ated with reduced risks of >/=30% decline in eGFR (hazard ratio [HR]: 0.77; 95% confidence interval [

131 ciated with lower risks of >/=30% decline in eGFR and AKI; rivaroxaban was associated with lower risk

132 to be independent predictors of a decline in eGFR at 1-year follow-up (-7.57%, p = 0.014; -6.39%, p =

133 We conclude that 30% decline in eGFR between years 1 and 3 after kidney transplant is co

134 22% of patients with HF had rapid decline in eGFR compared with 8.5% in patients without HF.

135 In conclusion, a mild-to-severe decline in eGFR or a raised level of BUN might be associated with i

136 ched a composite end point of 30% decline in eGFR or progression to ESRD over a median of 1.8 and 2.0

137 n, incident ESRD, and mean annual decline in eGFR than did NHW (P<0.05) but not NHB.

138 potential confounders, a 10-unit decline in eGFR was associated with higher risk for CHD (hazard rat

139 3 to 0.98] for >3 ml/min per year decline in eGFR), but not of incident CKD (incident rate ratio, 0.9

140 e interval, 0.66 to 0.93] for 30% decline in eGFR, and 0.85 [95% confidence interval, 0.73 to 0.98] f

141 mpared with stable eGFR, a >/=30% decline in eGFR, detected in 10% of patients, strongly associated w

142 4.0%, 14.8%, and 1.7% for >/=30% decline in eGFR, doubling of serum creatinine, AKI, and kidney fail

143 ciated with lower risks of >/=30% decline in eGFR, doubling of serum creatinine, and AKI; however, ap

144 R was negatively associated with declines in eGFR.

145 fined as the composite of >/=50% decrease in eGFR from baseline or ESRD, occurred in 15 intensive gro

146 al, 1.34 to 46.20) and an annual decrease in eGFR of >1 ml/min per 1.73 m(2) (odds ratio, 3.64; 95% c

147 incident CKD (defined as a >30% decrease in eGFR to a value <60 mL/min/1.73 m2), and a composite of

148 d for predonation factors, the difference in eGFR slopes between related and unrelated donors was 0.2

149 ixed-effects models to assess differences in eGFR slope.

150 stant, we noted a steady average increase in eGFR until donors reached age 70: 1.12 (95% CI: 0.92-1.3

151 e detected between bortezomib and placebo in eGFR slope (primary end point) was not significant (P=0.

152 ease was defined by a sustained reduction in eGFR less than 30 mL/min/1.73 m2 for at least 3 months d

153 primary outcome was ESRD or 50% reduction in eGFR.

154 ar mortality and of improvement/worsening in eGFR.

155 ml/min per year) and incident CKD (incident eGFR <60 ml/min per 1.73 m(2) and >1 ml/min per year dec

156 of PM2.5 concentrations and risk of incident eGFR <60 ml/min per 1.73 m(2), incident CKD, eGFR declin

157 other cardiovascular risk factors, including eGFR, and stronger after adjustment for the genotype of

158 d recipient eGFR suggests a risk of inferior eGFR with AKI versus no AKI (p < 0.005; OR 1.25 [95% CI:

159 ependent predictor of final eGFR was initial eGFR, highlighting the importance of early detection.

160 ed with individuals with normal eGFR levels (eGFR >/= 90 ml/min per 1.73 m(2)), individuals with a mi

161 evel measured at enrollment and longitudinal eGFR measured prospectively.

162 rogression was a composite of 50% eGFR loss, eGFR less than 10 mL/min/1.73 m2, or initiation of renal

163 nterval [95% CI], 1.07 to 3.08; P=0.03); low eGFR (<30 ml/min per 1.73 m(2)) at diagnosis (HR, 3.27;

164 Lower eGFR 1 year after kidney transplant is associated with s

165 age, blood pressure, proteinuria, and lower eGFR at baseline.

166 e found a gradient association between lower eGFR and higher likelihood of PPCs in the unadjusted mod

167 , men with classical Fabry disease had lower eGFR, higher left ventricular mass, and higher plasma gl

168 ersely correlated with RSF, suggesting lower eGFR for subjects with higher RSF (r = 0.24, p < 0.0001)

169 The difference in adjusted mean eGFR between the intensive and standard groups was -3.32

170 old, 37% of participants were men, and mean eGFR was 94 ml/min per 1.73 m(2) Over a median follow-up

171 f 59 participants with nondiabetic CKD (mean eGFR =37.6 ml/min per 1.73 m(2)) and 39 healthy control

172 itive patients had significantly higher mean eGFR than patients with negative C1q (p = 0.04).

173 Differences in mean eGFR during follow-up (estimated with a linear mixed-eff

174 had diabetes (mean age of 60 years old, mean eGFR =38 ml/min per 1.73 m(2), and median urine protein-

175 At last follow-up, mean eGFR was 50.2+/-26.1 ml/min per 1.73 m(2)with 9% of pati

176 +/-SD) years of age and 24% were women; mean eGFR was 38+/-13 ml/min per 1.73 m(2) Compared with plac

177 trol subjects (mean age: 60+/-11 years, mean eGFR: 86+/-16 ml/min per 1.73 m(2)).

178 Mean+/-eGFR was 39.5+/-20.4 ml/min per 1.73 m(2) Membranoprolif

179 The median eGFR was 56 mL/min (range, 35 to 135 mL/min).

180 were associated with lower adjusted 12-month eGFR (95% confidence interval)-by 7.3 (3.6-10.9) and 7.4

181 Adjusted relative risks for 12-month eGFR less than 30 mL/min per 1.73 m were 1.9 (1.2-3.1) a

182 had the strongest association with 12-month eGFR, and POD5 creatinine and creatinine reduction betwe

183 day 7 creatinine is correlated with 12-month eGFR, but large translational studies are needed to unde

184 t-based SGF definitions relative to 12-month eGFR.

185 demonstrated modest separations in 12-month eGFR.

186 concentration associated with higher 6-month eGFR (6.75 [95% CI, 1.49 to 12.02] ml/min per 1.73 m(2))

187 tions associated with slightly lower 6-month eGFR only among recipients without delayed graft functio

188 week post-transplant), and recipient 6-month eGFR.

189 1.09); compared with individuals with normal eGFR levels (eGFR >/= 90 ml/min per 1.73 m(2)), individu

190 e level (HR, 1.53; 95% CI, 1.42 to 1.65), of eGFR decline >30% (HR, 1.32; 95% CI, 1.28 to 1.37), and

191 Analysis of eGFR and htTKV measures showed that patients with MSG3 b

192 on models to investigate the associations of eGFR and BUN with risk of incident CHD in the prospectiv

193 atheterization and estimated associations of eGFR with the renal elimination of metabolites.

194 utcomes were consistent across categories of eGFR and urine albumin-creatinine ratio at baseline and

195 The annual rate of change of eGFR was -3.1 mL/min/1.73 m(2) per year (95% CI -2.9 to

196 significantly greater yearly mean decline of eGFR (Ptrend<0.001) and rise of cystatin C (Ptrend=0.01)

197 The annualized loss of eGFR was inversely associated with baseline 25(OH)D leve

198 1972 and 2014) with baseline measurements of eGFR and albuminuria, at least 1000 participants (this c

199 incident CKD or mortality, and rapid rate of eGFR decline (slopes steeper than -5 mL min(-1) 1.73 m(-

200 n) and examined post hoc the relationship of eGFR with end points across treatment arms.

201 independently associated with higher risk of eGFR decline in persons with early or advanced DKD.

202 An increased risk of eGFR of less than 60 mL/min per 1.73 m(2) was associated

203 ration was associated with increased risk of eGFR<60 ml/min per 1.73 m(2) (hazard ratio [HR], 1.21; 9

204 associated with similarly increased risk of eGFR<60 ml/min per 1.73 m(2), CKD, eGFR decline >/=30%,

205 resent epigenome-wide association studies of eGFR and CKD using whole-blood DNA methylation of 2264 A

206 used to model the longitudinal trajectory of eGFR.

207 population, because it has a large effect on eGFR and CKD risk that is consistent across different et

208 tion and highlighted that allelic effects on eGFR at lead SNPs are homogeneous across ancestries.

209 to 3.8, respectively) and albuminuria and/or eGFR<60 ml/min per 1.73 m(2) (OR, 2.9; 95% CI, 1.5 to 5.

210 (urinary protein/creatinine ratio >4 g/g or eGFR<45 ml/min per 1.73 m(2) at end of follow-up).

211 g/dl for women and 1.5-3.5 mg/dl for men (or eGFR of 20-60 ml/min per 1.73 m(2)), and a 24-hour urine

212 h a 5-mL/min/1.73 m decrease of postdonation eGFR after adjusting for donor age at donation, sex, rac

213 We compared long-term postdonation eGFR trajectory for donors with (n = 1245) vs. without (

214 rative systolic blood pressure, preoperative eGFR, and time since donation (P < 0.01).

215 Among patients with preoperative eGFR>/=30 ml/min per 1.73 m(2), the incidence of CKD sta

216 KD, composite of CKD or mortality, and rapid eGFR decline, respectively.

217 nt CKD, incident CKD or mortality, and rapid eGFR decline.

218 educed estimated glomerular filtration rate (eGFR <60 mL/min/1.73 m2), and severely reduced eGFR (<30

219 e, and estimated glomerular filtration rate (eGFR) >/=30 mL.min(-1).1.73 m(-2) at screening were rand

220 s with estimated glomerular filtration rate (eGFR) >/=60 mL min(-1) 1.73 m(-2) during October 1, 2004

221 erived estimated glomerular filtration rate (eGFR) and assessment of proteinuria in spot or timed uri

222 Estimated glomerular filtration rate (eGFR) has been reported to be associated with risk of in

223 on the estimated glomerular filtration rate (eGFR) in 110,517 European ancestry participants using 10

224 ith an estimated glomerular filtration rate (eGFR) of 40 mL/min or greater were randomly assigned 1:1

225 ith an estimated glomerular filtration rate (eGFR) of 40 mL/min or greater were randomly assigned 1:1

226 seline estimated glomerular filtration rate (eGFR) of at least 60 mL/min/1.73 m2.

227 cident estimated glomerular filtration rate (eGFR) of less than 60 mL/min per 1.73 m(2), incident chr

228 zation estimated glomerular filtration rate (eGFR) of more than 45 mL/min/1.73 m2 and who had survive

229 e mean estimated glomerular filtration rate (eGFR) was 33.9 +/- 15.8 ml/min/1.73 m(2) and the median

230 nge of estimated glomerular filtration rate (eGFR) with off-treatment nucleos(t)ide analogues (NA) in

231 rative estimated glomerular filtration rate (eGFR) with PPCs in laparoscopic surgeries.

232 /PNF), estimated glomerular filtration rate (eGFR), and graft-survival at 90 days and 1 year was anal

233 ine in estimated glomerular filtration rate (eGFR), doubling of the serum creatinine level, acute kid

234 educed estimated glomerular filtration rate (eGFR), has been associated with increased risk of corona

235 terol, estimated glomerular filtration rate (eGFR), incident microalbuminuria (not reported), inciden

236 CI and estimated glomerular filtration rate (eGFR), such that higher CI was paradoxically associated

237 ut not estimated glomerular filtration rate (eGFR), was associated with increased WMH burdens (p = 0.

238 -month estimated glomerular filtration rate (eGFR).

239 n with estimated glomerular filtration rate (eGFR).

240 nge of estimated glomerular filtration rate (eGFR).

241 educed estimated glomerular filtration rate (eGFR).

242 nes in estimated glomerular filtration rate (eGFR).

243 Estimated glomerular filtration rate (eGFR, a marker of kidney function) and serum PFOA concen

244 rment (estimated glomerular filtration rate [eGFR] </= 60 mL/min) and paired baseline and 30-day meas

245 firmed estimated glomerular filtration rate [eGFR] </= 60 ml/min/1.73 m2) events in HIV-positive peop

246 rment (estimated glomerular filtration rate [eGFR] <60 mL/min/1.73m2), albuminuria (albumin/creatinin

247 sease (estimated glomerular filtration rate [eGFR] and albuminuria) with the incidence of peripheral

248 (CKD) (estimated glomerular filtration rate [eGFR], >/= 60 mL/min/1.73 m(2)), those with stage 3 CKD

249 sis of association between AKI and recipient eGFR suggests a risk of inferior eGFR with AKI versus no

250 ing systems for CKD account for both reduced eGFR and albuminuria; whether each measure associates wi

251 erapy in individuals with moderately reduced eGFR (30-60 ml/min per 1.73 m(2)).

252 FR <60 mL/min/1.73 m2), and severely reduced eGFR (<30 mL/min/1.73 m2), incorporating data on biologi

253 did tubulopathy predict clinically relevant eGFR decline.

254 CKD (mean+/-SD age: 59+/-5 years, mean+/-SD eGFR: 37+/-12 ml/min per 1.73 m(2)) but without cardiova

255 ariants PEPT2*1/*2 and PEPT2*2/*2 (mean+/-SD eGFR: 54.4+/-19.1, 66.6+/-23.8, and 78.1+/-19.9 ml/min p

256 .73 m(2)), individuals with a mild-to-severe eGFR decline (15 to 60 ml/min per 1.73 m(2)) were at sig

257 Compared with stable eGFR, a >/=30% decline in eGFR, detected in 10% of patie

258 ses each year for a number of years and that eGFR trajectory does not explain any increase in ESRD af

259 The eGFR was 60 mL/min or lower among 821 patients (72%), of

260 ase Epidemiology Collaboration equation, the eGFR was estimated from cystatin C with all available sa

261 The new model improved the eGFR accuracy (RMSE, 15.00 mL/min; 95% CI, 14.12 to 16.0

262 s associated with less annual decline in the eGFR (P-trend = 0.003).

263 these associations, but the PPCs risk in the eGFR groups of <30, 30-60, and >/=120 mL/min/1.73 m(2) r

264 Analysis of the eGFR and htTKV measures showed that the PKD1 group had m

265 decline of renal function independent of the eGFR formula used.

266 653) of those with CKD G3aA1 by eGFRcreat to eGFR >/= 60 ml/min/1.73 m2.

267 a positive effect on average post-transplant eGFR and balanced out the negative effect of recipient/d

268 -2013 period, average 1-year post-transplant eGFR remained essentially unchanged, with differences of

269 n conclusion, average 1-year post-transplant eGFR remained stable, despite increasingly unfavorable a

270 tice changes on the national post-transplant eGFR trend.

271 age, preservation of average post-transplant eGFR will require sustained improvement in immunosuppres

272 rger temporal improvement in post-transplant eGFR.

273 3.97 (1.37-11.5), p = 0.01) and pre-treated eGFR (OR, 0.98 (0.95-1.00), p = 0.04).

274 study is aimed to evaluate the off-treatment eGFR after 3 years of therapy with telbivudine (LdT) or

275 alysis, the predictors for the off-treatment eGFR improvement were the LdT treatment (odds ratio [OR]

276 gorized with improved eGFR (30-day follow-up eGFR>/=10% higher than baseline pre-TAVR), worsened eGFR

277 mg/g or dipstick proteinuria 2+ or higher vs eGFR >/=90 mL/min per 1.73 m(2) plus ACR <10 mg/g or dip

278 es significantly associated (P < 1e-07) with eGFR/CKD and replicated, five also associate with renal

279 Of these 53 loci, 19 associate with eGFR among individuals with diabetes.

280 larly, rs931891 in LINC00923 associated with eGFR decline (P=1.44x10(-4)) in white patients without d

281 SNP, rs653178, which was not associated with eGFR in the UCLEB sample, but has known pleiotropic effe

282 genetic variants previously associated with eGFR to investigate the causal role of kidney function o

283 The absence of an association with eGFR changes suggests that the higher eGFR among coffee

284 threshold of P<1x10(-6) for association with eGFR slope were selected as candidates for follow-up and

285 etylglutamine clearance also correlated with eGFR (rho=0.84; P<0.001).

286 ular secretion rate modestly correlated with eGFR and associated with some participant characteristic

287 , glycosylation modification correlated with eGFR loss.

288 ction of parathyroid hormone correlated with eGFR.

289 ificant correlation of HIF-target genes with eGFR in glomeruli and tubulointerstitium.

290 (CRIC) study enrolled 3939 participants with eGFR<70 ml/min per 1.73 m(2) from June 2003 to September

291 nt profile of empagliflozin in patients with eGFR <60 mL.min(-1).1.73 m(-2) was consistent with the o

292 ACR grouping as the referent, patients with eGFR=15 to <30 ml/min per 1.73 m(2) had adjusted relativ

293 th all-cause mortality only in subjects with eGFR <90 mL/min/1.73 m(2) [adjusted HR:1.18 (95% CI, 1.0

294 use mortality, particularly in subjects with eGFR <90 mL/min/1.73 m(2).

295 r CI was paradoxically associated with worse eGFR (r = -0.12; p = 0.02).

296 10% higher than baseline pre-TAVR), worsened eGFR (>/=10% lower), or no change in renal function (nei

297 pants with improved, unchanged, or worsening eGFR was 84.90 (6.91) years, 84.37 (7.13) years, and 85.

298 R did not improve 1-year outcomes, worsening eGFR was associated with increased mortality.

299 Those with worsening eGFR had a higher median Society of Thoracic Surgeons sc

300 Those with worsening eGFR had increased mortality (25.5% vs 19.1%, P = .07) b